Related Experiment Video
Updated: Aug 25, 2026
High Throughput Sequential ELISA for Validation of Biomarkers of Acute Graft-Versus-Host Disease
Published on: October 31, 2012
[Serum cytokine profiles in stable survivors with clinical liver transplantation]
Yun-le Wan1, Shu-sen Zheng, Jian-feng Wei
1Department of Hepatobiliary Pancreatic Surgery, Key lab of Combined Multi-organ Transplantation, Ministry of Public Health, First Affiliated Hospital, Zhejiang University Medical College, Hangzhou 310003, China.
Objective:
To elucidate the profile of serum cytokines and adhesion molecules in stable survivors with clinical liver transplantation.
Methods:
Flow cytometric analysis was used to analyse the phenotype of T cell subsets in peripheral blood mononuclear cells (PBMCs) from group of liver transplantation (LTx) (n = 22), primary liver carcinoma (PLC) (n = 13) and healthy control (n = 12). Enzyme-linked immunoabsorbent assay (ELISA) was used to determine the serum cytokines and adhesion molecules profiles in stable survivors with clinical liver transplantation.
Results:
Percentage of CD3(+) T cell and CD8(+) T cell, as well as ratio of CD4(+) to CD8(+) revealed no difference among three groups. The percentage of CD3(+)CD25(+) T cells in LTx group was found higher than that in healthy group (P = 0.022). Th1 cytokines (IL-2, IFN-gamma) and Th2 cytokines (IL-4, IL-10), as well as TNF-alpha displayed no significant difference among three groups. The levels of IL-6, ICAM-1 and P-selectin in serum were not found any difference between LTx group and PLC group, while the levels of IL-6, ICAM-1 and P-selectin in serum shown significant difference between LTx and healthy groups (P = 0.048, 0.000 and 0.025, respectively).
Conclusions:
Our data demonstrates that effector T-cells can also be activated and exert immunoresponse to grafts permanently under the treatment of immunosuppressant. Adhesion molecules (ICAM-1, P-Selectin) and pro-inflammatory cytokines (IL-6, TNF-alpha) might be involved in the process of chronic graft damage induced by allo-immunoresponse.
